Korean J Urol.  2009 Oct;50(10):1014-1017.

Clinical Significance of Infected Prostate Tissue in Patients with Benign Prostatic Hyperplasia

• Choi H
• Park SC
• Jeong HJ
• Jo JH

Abstract

PURPOSE
Benign prostatic hyperplasia (BPH) and prostatitis are the most common benign diseases of the prostate gland and over time affect a significant majority of men. We evaluated the relation between BPH and infection in prostatic tissue in men who underwent transurethral resection of the prostate (TURP).
MATERIALS AND METHODS
This prospective study included 63 consecutive patients diagnosed with BPH and scheduled for TURP. During the TURP, 1-2 g chips were collected after resection of the prostatic urethra, and specimens were transported to the laboratory in sterile saline. Homogenized specimens were incubated for 7 days. The patients were divided into 2 groups (group 1: culture positive, group 2: culture negative). We compared prostate volume, prostate calculi, serum prostate-specific antigen (PSA), International Prostate Symptom Score (IPSS), maximum flow rate (Qmax), post-void residual urine, and ratio of the transitional zone prostate to total prostate (transitional zone ratio).
RESULTS
Mean age was 72 years and mean serum PSA was 4.36 ng/dl. Group 1 included 7 patients (11.1%) and group 2 included 57 patients (88.9%). There were no significant differences in prostate volume, prostate calculi, serum PSA, IPSS, Qmax, or post-void residual urine between groups, but the transitional zone ratio was higher in group 1 (45.4%) than in group 2 (30.3%) (p<0.05).
CONCLUSIONS
About 11% of the prostate tissue cultures showed bacterial growth. The transitional zone ratio was higher in patients with bacteria growth. Bacterial infection may be related to benign prostatic hyperplasia.

Keyword

Prostatic hyperplasia; Prostatitis; Inflammation

MeSH Terms

Bacteria
Bacterial Infections
Calculi
Humans
Inflammation
Male
Prospective Studies
Prostate
Prostate-Specific Antigen
Prostatic Hyperplasia
Prostatitis
Transurethral Resection of Prostate
Urethra
Prostate-Specific Antigen

Reference

1.Holtgrewe HL. Current trends in management of men with lower urinary tract symptoms and benign prostatic hyperplasia. Urology. 1998. 51(4A Suppl):1–7.

2.McNicholas TA. Lower urinary tract symptoms suggestive of benign prostatic obstruction: What are the current practice patterns? Eur Urol. 2001. 39(Suppl 3):26–30.

3.Collins MM., Stafford RS., O'Leary MP., Barry MJ. How common is prostatitis? A national survey of physician visits. J Urol. 1998. 159:1224–8.

4.Roberts RO., Lieber MM., Rhodes T., Girman CJ., Bostwick DG., Jacobsen SJ. Prevalence of a physician-assigned diagnosis of prostatitis: the Olmsted County Study of Urinary Symptoms and Health Status Among Men. Urology. 1998. 51:578–84.

5.Woo YN. Prostatitis. Korean J Urol. 1994. 35:575–85.

6.Kohnen PW., Drach GW. Pattern of inflammation in prostatic hyperplasia: a histologic and bacteriologic study. J Urol. 1979. 121:755–60.

7.Nickel JC., Downey J., Young I., Boag S. Asymptomatic inflammation and/or infection in benign prostatic hyperplasia. BJU Int. 1999. 84:976–81.

8.Krieger JN., Nyberg L Jr., Nickel JC. NIH consensus definition and classification of prostatitis. JAMA. 1999. 282:236–7.

9.Collins MM., Stafford RS., O'Leary MP., Barry MJ. Distinguishing chronic prostatitis and benign prostatic hyperplasia symptoms: results of a national survey of physician visits. Urology. 1999. 53:921–5.

10.Roehrborn CG., Kaplan SA., Nobel WD., Slawin KM., McVary KT., Kusek JW. The impact of acute or chronic inflammation in baseline biopsy on the risk of clinical progression of BPH. Results from the MTOPS study. J Urol. 2005. 173(Suppl):346.

11.Krieger JN., Riley DE. Prostatitis: what is the role of infection. Int J Antimicrob Agents. 2002. 19:475–9.

12.Naber KG., Weidner W. Chronic prostatitis-an infectious disease? J Antimicrob Chemother. 2000. 46:157–61.

13.Krieger JN., Riley DE., Roberts MC., Berger RE. Prokaryotic DNA sequences in patients with chronic idiopathic prostatitis. J Clin Microbiol. 1996. 34:3120–8.

14.Krieger JN., Riley DE. Bacteria in the chronic prostatitis-chronic pelvic pain syndrome: molecular approaches to critical research questions. J Urol. 2002. 167:2574–83.

15.Mishra VC., Allen DJ., Nicolaou C., Sharif H., Hudd C., Karim OM, et al. Does intraprostatic inflammation have a role in the pathogenesis and progression of benign prostatic hyperplasia? BJU Int. 2007. 100:327–31.

16.Lee SO., Cho IR., Lee KC., Kim HS. Elevation of serum prostate specific antigen in subclinical prostatitis: the role of pathology of inflammation. Korean J Urol. 2006. 47:31–6.

17.Kramer G., Marberger M. Could inflammation be a key component in the progression of benign prostatic hyperplasia? Curr Opin Urol. 2006. 16:25–9.

18.Berger RE., Krieger JN., Rothman I., Muller CH., Hillier SL. Bacteria in the prostate tissue of men with idiopathic prostatic inflammation. J Urol. 1997. 157:863–5.

19.Kramer G., Steiner GE., Handisurya A., Stix U., Haitel A., Knerer B, et al. Increased expression of lymphocyte-derived cytokines in benign hyperplastic prostate tissue, identification of the producing cell types, and effect of differentially expressed cytokines on stromal cell proliferation. Prostate. 2002. 52:43–58.

20.Kessler OJ., Keisari Y., Servadio C., Abramovici A. Role of chronic inflammation in the promotion of prostatic hyperplasia in rats. J Urol. 1998. 159:1049–53.